Signaling pathways bridging microbial-triggered inflammation and cancer

Kipanyula, Maulilio J.; Etet, Paul Faustin Seke; Vecchio, Lorella; Farahna, Mohammed; Nukenine, Elias Nchiwan; Kamdje, Armel Hervé Nwabo

doi:10.1016/j.cellsig.2012.10.014

Cited by 106 publications

(79 citation statements)

References 164 publications

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“…Moreover, EPEC infection can activate PKCα, phosphorylate Bcl-2 and inhibit the transcription of MMR genes [86]. A/E E. coli infected intestinal epithelial cells by injecting toxic proteins, leading to DNA damage in host cells, and, together with the Toll-like receptor signaling pathway, the NF-κB pathway and other cell inflammatory pathways, accelerated the process of cancer [86][87][88]. A/E E. coli can regulate the expression of DNA mismatch repair protein in host cells by post-transcriptional manipulation of EspF protein, causing a decrease in host cell MMR protein levels, EspF entered the host cell, targeting binding to mitochondria, leading to Apc and MMR protein gene mutations [57], and may even activate kras and other oncogenes, leading to changes in intestinal epithelium, causing colitis and even colorectal carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Screening for Host Proteins Interacting with Escherichia Coli O157:H7 EspF using Bimolecular Fluorescence Complementation

Hua

Wang

et al. 2017

Future Microbiol.

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Aim:To screen host proteins that interact with enterohemorrhagic Escherichia coli O157:H7 EspF. Materials & methods: Flow cytometry and high-throughput sequencing were used to screen interacting proteins. Molecular function, biological processes and Kyoto Encyclopedia of Genes and Genomes pathways were studied using the DAVID online tool. Glutathione S-transferase pull down and dot blotting were used to verify the interactions. Results: 293 host proteins were identified to associate with EspF. They were mainly enriched in RNA splicing (p = 0.005), ribosome structure (p = 0.012), and involved in 109 types of signaling pathways. SNX9 and ANXA6 were confirmed to interact with EspF. Conclusion: EspF interacts with ANXA6; they may form a complex to manipulate the process of phagocytosis; EspF plays a highlighted pathogenic role in enterohemorrhagic E. coli infection process. Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an important food-borne causative agent in sporadic outbreaks of illness such as diarrhea, hemorrhagic colitis and hemolytic-uremic syndrome. Severe symptoms may even lead to death [1][2][3][4]. Research into EHEC has mainly explored the development of attaching and effacing (A/E) intestinal lesions and the secretion of Shiga toxin in EHEC infection [5][6][7]. The protein EspF is one of the multifunctional effectors of A/E lesions induced by EHEC and enteropathogenic E. coli (EPEC). EspF participates in a number of damage processes in host cells, targeting mitochondria and nucleoli [6,8] and disrupting the tight junctions (TJs) of intestinal epithelial cells [9], leading to cytoskeletal rearrangements, actin polymerization and pedestal formation [10]. EspF thus emerges as the 'Swiss army knife' of a bacterial pathogen [11,12]. EHEC O157:H7 employs a type-III secretion system to export toxic factors and effector proteins to host cells after adhering to the brush border of epithelial cells [5,[13][14]. The production of virulence factors, subsequent invasion and diffusion, and the interaction of effector proteins with host proteins are key steps in EHEC O157:H7 pathogenesis. The mechanism by which EspF breaks through the intestinal epithelial barrier into host cells, the host proteins that EspF interacts with, and how cellular damage, and even apoptosis, result remain unclear. Studying the pathogen-host interaction process will increase the emerging knowledge about EHEC O157:H7 pathogenesis.The EspF protein has been shown to induce apoptosis after 'injection' into host cells [1]. The N-terminal (1-73 amino acids [aa]) of this approximately 27 kDa protein contains a secretory signal (1-20 aa), a mitochondrialtargeting signal (1-24 aa) and a nucleolar-targeting domain (21-74 aa); 73-248 aa consists of four proline-rich repeats (PRRs), each containing a eukaryotic cell sorting nexin 9 (SNX9) protein-binding site SH3 motif, an

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Section: Discussionmentioning

confidence: 99%

Screening for Host Proteins Interacting with Escherichia Coli O157:H7 EspF using Bimolecular Fluorescence Complementation

Hua

Wang

et al. 2017

Future Microbiol.

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“…The knowledge of these microbial species is rapidly developing, and further understanding will require metagenomic and proteomic studies. These discoveries in the microbiology of infectious diseases will have an impact on the identification of known and new microorganisms involved in chronic diseases such as cancer (Kipanyula et al 2013).…”

Section: Resultsmentioning

confidence: 99%

“…It is possible for bacteria to enter the bloodstream, for example, from periodontitis, untreated carious lesions, or wound healing. Members of the human microbiota community play an active role in carcinogenesis through DNA damage (as is the case with Escherichia coli) (Su et al 2015) and chronic infection (as is the case with Helicobacter pylori) (Kipanyula et al 2013).…”

Section: Introductionmentioning

confidence: 99%

The oral cavity microbiota: between health, oral disease, and cancers of the aerodigestive tract

et al. 2017

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Many studies show that the human microbiome plays a critical role in the chronic pathologies of obesity, inflammatory bowel diseases, and diabetes. More recently, the interaction between cancer and the microbiome has been highlighted. Most studies have focused on the gut microbiota because it represents the most extensive bacterial community, and the body of evidence correlating it with gut syndromes is increasing. However, in the strict sense, the gastrointestinal (GI) tract begins in the oral cavity, and special attention should be paid to the specific flora of this cavity. This study reviewed the current knowledge about the various microbial ecosystems of the upper part of the GI tract and discussed their potential link to carcinogenesis. The overall composition of the microbial communities, as well as the presence or absence of "key species", in relation to carcinogenesis is addressed. Alterations in the oral microbiota can potentially be used to predict the risk of cancer. Molecular advances and the further monitoring of the microbiota will increase our understanding of the role of the microbiota in carcinogenesis and open new perspectives for future therapeutic and prophylactic modalities.Key words: upper aerodigestive, microbiome, oral cavity, carcinogenesis.Résumé : Plusieurs études montrent que le microbiome humain joue un rôle essentiel dans les pathologies chroniques que sont l'obésité, les maladies inflammatoires de l'intestin et le diabète. Plus récemment, l'interaction entre le cancer et le microbiome a été soulignée. La plupart des études se sont concentrées sur le microbiote intestinal car il représente la communauté bactérienne la plus étendue, et l'ensemble des preuves le corrélant avec les syndromes de l'intestin est en croissance. Cependant, au sens strict, le tractus gastro-intestinal (GI) commence dans la cavité orale et une attention spéciale devrait être portée à la flore spécifique de cette cavité. Cette étude fait la synthèse des connaissances actuelles relatives à divers écosystèmes microbiens de la partie supérieure du tractus GI et discute de leur lien potentiel à la carcinogenèse. La composition globale des communautés microbiennes, de même que la présence ou l'absence « d'espèces clés » relativement à la carcinogenèse sont soulevées. Des modifications du microbiote oral peuvent potentiellement être utilisées pour prédire les risques de cancer. Les percées moléculaires et la surveillance accrue du microbiote accroitront notre compréhension du rôle du microbiote dans la carcinogenèse et ouvriront de nouvelles perspectives en vue de modalités thérapeutiques et prophylactiques futures. [Traduit par la Rédaction]

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“…It is noteworthy that it is not only the bacterial dysbiosis but also the biometabolites of altered bacteria that are involved in the transition from acute to chronic inflammation and IBD (Kipanyula et al, 2013).…”

Section: F Nucleatum and Inflammatory Bowel Diseasementioning

confidence: 99%

Fusobacterium nucleatum

Bashir

Miskeen²,

Bhat³

et al. 2015

European Journal of Cancer Prevention

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The human intestinal microbiota is a plethora of diverse microbial species, wherein certain bacteria considered as driver bacteria with procarcinogenic features contribute directly toward colonic epithelium cell damage to initiate colorectal carcinogenesis. However, some bacteria, in particular Fusobacterium nucleatum, which is otherwise a normal resident of the oral microflora and a relatively poor colonizer of the healthy gut, have also been considered to play a role in the development of colorectal cancer. Many studies have reported that F. nucleatum is associated with colorectal adenomas and advanced-stage colorectal cancer, but its precise role in the early stages of colorectal tumorigenesis is poorly understood. Here, we review some of the important features of F. nucleatum, its association with inflammatory bowel disease, modulation of the tumor-immune microenvironment, and E-cadherin/β-catenin signaling.

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Signaling pathways bridging microbial-triggered inflammation and cancer

Cited by 106 publications

References 164 publications

Screening for Host Proteins Interacting with Escherichia Coli O157:H7 EspF using Bimolecular Fluorescence Complementation

Screening for Host Proteins Interacting with Escherichia Coli O157:H7 EspF using Bimolecular Fluorescence Complementation

The oral cavity microbiota: between health, oral disease, and cancers of the aerodigestive tract

Fusobacterium nucleatum

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